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Publication : The Sympathetic Nervous System Mitigates CNS Autoimmunity via β2-Adrenergic Receptor Signaling in Immune Cells.

First Author  Araujo LP Year  2019
Journal  Cell Rep Volume  28
Issue  12 Pages  3120-3130.e5
PubMed ID  31533035 Mgi Jnum  J:298022
Mgi Id  MGI:6457177 Doi  10.1016/j.celrep.2019.08.042
Citation  Araujo LP, et al. (2019) The Sympathetic Nervous System Mitigates CNS Autoimmunity via beta2-Adrenergic Receptor Signaling in Immune Cells. Cell Rep 28(12):3120-3130.e5
abstractText  Noradrenaline (NE), the main neurotransmitter released by sympathetic nerve terminals, is known to modulate the immune response. However, the role of the sympathetic nervous system (SNS) on the development of autoimmune diseases is still unclear. Here, we report that the SNS limits the generation of pathogenic T cells and disease development in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). beta2-Adrenergic receptor (Adrb2) signaling limits T cell autoimmunity in EAE through a mechanism mediated by the suppression of IL-2, IFN-gamma, and GM-CSF production via inducible cAMP early repressor (ICER). Accordingly, the lack of Adrb2 signaling in immune cells is sufficient to abrogate the suppressive effects of SNS activity, resulting in increased pathogenic T cell responses and EAE development. Collectively, these results uncover a suppressive role for the SNS in CNS autoimmunity while they identify potential targets for therapeutic intervention.
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